ArticleInfection and immunity2003
Killing of Candida albicans by human salivary histatin 5 is modulated, but not determined, by the potassium channel TOK1.
Article in Infection and immunity, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
- Ovotransferrin and Its γ-Core-Containing Peptides Impair Pma1-Dependent Proton Homeostasis inInternational journal of molecular sciences · 2026Article
- Antimicrobial Effect of Silver Nanoparticles Capped withNanomaterials (Basel, Switzerland) · 2026Article
- Article
- The KillerMicroorganisms · 2024Review
- Zinc Binding Inhibits Cellular Uptake and Antifungal Activity of Histatin-5 inACS infectious diseases · 2022Article
- Review
- TOK channels use the two gates in classical KFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Cytosolic Acidification Is the First Transduction Signal of Lactoferrin-induced Regulated Cell Death Pathway.International journal of molecular sciences · 2019Article
- Promising Antifungal Targets AgainstFrontiers in cellular and infection microbiology · 2018Review
- Antifungal Activity and Action Mechanism of Histatin 5-Halocidin Hybrid Peptides against Candida ssp.PloS one · 2016Article
- A new look at the antibiotic amphotericin B effect on Candida albicans plasma membrane permeability and cell viability functions.European biophysics journal : EBJ · 2015Article
- Identification and mechanism of action of the plant defensin NaD1 as a new member of the antifungal drug arsenal against Candida albicans.Antimicrobial agents and chemotherapy · 2013Article
- Article
- Salivary histatin 5 internalization by translocation, but not endocytosis, is required for fungicidal activity in Candida albicans.Molecular microbiology · 2010Article
- Candida albicans cell wall proteins.Microbiology and molecular biology reviews : MMBR · 2008Review
- The role of released ATP in killing Candida albicans and other extracellular microbial pathogens by cationic peptides.Purinergic signalling · 2007Article
- Synthetic histidine-rich peptides inhibit Candida species and other fungi in vitro: role of endocytosis and treatment implications.Antimicrobial agents and chemotherapy · 2006Article
- In the yeast potassium channel, Tok1p, the external ring of aspartate residues modulates both gating and conductance.Pflugers Archiv : European journal of physiology · 2005Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Salivary histatin 5 (Hst 5), a potent toxin for the human fungal pathogen Candida albicans, induces noncytolytic efflux of cellular ATP, potassium, and magnesium in the absence of cytolysis, implicating these ion movements in the toxin's fungicidal activity. Hst 5 action on Candida resembles, in many respects, the action of the K1 killer toxin on Saccharomyces cerevisiae, and in that system the yeast plasma membrane potassium channel, Tok1p, has recently been reported to be a primary target of toxin action. The question of whether the Candida homologue of Saccharomyces Tok1p might be a primary target of Hst 5 action has now been investigated by disruption of the C. albicans TOK1 gene. The resultant strains (TOK1/tok1) and (tok1/tok1) were compared with wild-type Candida (TOK1/TOK1) for relative ATP leakage and killing in response to Hst 5. Patch-clamp measurements on Candida protoplasts were used to verify the functional deletion of Tok1p and to provide its first description in Candida. Tok1p is an outwardly rectifying, noisily gated, 40-pS channel, very similar to that described in Saccharomyces. Knockout of CaTOK1 (tok1/tok1) completely abolishes the currents and gating events characteristic of Tok1p. Also, knockout (tok1/tok1) increases residual viability of Candida after Hst 5 treatment to 27%, from 7% in the wild type, while the single allele deletion (TOK1/tok1) increases viability to 18%. Comparable results were obtained for Hst-induced ATP efflux, but quantitative features of ATP loss suggest that wild-type TOK1 genes function cooperatively. Overall, very substantial killing and ATP efflux are produced by Hst 5 treatment after complete knockout of wild-type TOK1, making clear that Tok1p channels are not the primary site of Hst 5 action, even though they do play a modulating role.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.